Lipoxygenase metabolism : roles in tumor progression and survival
Pidgeon, Graham P., Lysaght, Joanne, Krishnamoorthy, Sriram, Reynolds, John V., O'Byrne, Kenneth J., Nie, Daotie, & Honn, Kenneth V. (2007) Lipoxygenase metabolism : roles in tumor progression and survival. Cancer and Metastasis Reviews, 26(3-4), pp. 503-524.
The metabolism of arachidonic acid through lipoxygenase pathways leads to the generation of various biologically active eicosanoids. The expression of these enzymes vary throughout the progression of various cancers, and thereby they have been shown to regulate aspects of tumor development. Substantial evidence supports a functional role for lipoxygenase-catalyzed arachidonic and linoleic acid metabolism in cancer development. Pharmacologic and natural inhibitors of lipoxygenases have been shown to suppress carcinogenesis and tumor growth in a number of experimental models. Signaling of hydro[peroxy]fatty acids following arachidonic or linoleic acid metabolism potentially effect diverse biological phenomenon regulating processes such as cell growth, cell survival, angiogenesis, cell invasion, metastatic potential and immunomodulation. However, the effects of distinct LOX isoforms differ considerably with respect to their effects on both the individual mechanisms described and the tumor being examined. 5-LOX and platelet type 12-LOX are generally considered pro-carcinogenic, with the role of 15-LOX-1 remaining controversial, while 15-LOX-2 suppresses carcinogenesis. In this review, we focus on the molecular mechanisms regulated by LOX metabolism in some of the major cancers. We discuss the effects of LOXs on tumor cell proliferation, their roles in cell cycle control and cell death induction, effects on angiogenesis, migration and the immune response, as well as the signal transduction pathways involved in these processes. Understanding the molecular mechanisms underlying the anti-tumor effect of specific, or general, LOX inhibitors may lead to the design of biologically and pharmacologically targeted therapeutic strategies inhibiting LOX isoforms and/or their biologically active metabolites, that may ultimately prove useful in the treatment of cancer, either alone or in combination with conventional therapies. © 2007 Springer Science+Business Media, LLC.
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|Item Type:||Journal Article|
|Keywords:||Angiogenesis, Apoptosis, Immune suppression, Lipoxygenase, Tumor survival, 2 [2 propyl 3 [3 [2 ethyl 4 (4 fluorophenyl) 5 hydroxyphenoxy]propoxy]phenoxy]benzoic acid, 3 [3 tert butylthio 1 (4 chlorobenzyl) 5 isopropyl 2 indolyl] 2, 2 dimethylpropionic acid, arachidonate 12 lipoxygenase, arachidonate 15 lipoxygenase, arachidonate 3 lipoxygenase, arachidonate 5 lipoxygenase, arachidonate 8 lipoxygenase, arachidonic acid, baicalein, celecoxib, ciglitazone, cisplatin, cyclooxygenase 2, cyclooxygenase 2 inhibitor, gemcitabine, indometacin, isotretinoin, kaempferol, linoleic acid, lipoxygenase inhibitor, nonsteroid antiinflammatory agent, nordihydroguaiaretic acid, paclitaxel, phospholipase A2, phospholipid, prostaglandin synthase inhibitor, quercetin, resveratrol, thromboxane A2, unclassified drug, breast cancer, carcinogenesis, cell growth, cell survival, chemoprophylaxis, colon cancer, enzyme mechanism, enzyme metabolism, human, immunomodulation, low drug dose, lung non small cell cancer, melanoma, nonhuman, priority journal, prostate cancer, protein analysis, protein expression, protein function, regulatory mechanism, review, signal transduction, stomach cancer, tea, thyroid cancer, tumor growth, Animals, Cell Movement, Cell Proliferation, Disease Progression, Humans, Immune System, Lipoxygenase Inhibitors, Neoplasm Invasiveness, Neoplasms, Neovascularization, Pathologic, Prostaglandin-Endoperoxide Synthases|
|Divisions:||Current > Schools > School of Biomedical Sciences
Current > QUT Faculties and Divisions > Faculty of Health
Current > Institutes > Institute of Health and Biomedical Innovation
|Copyright Owner:||Copyright 2007 Springer New York LLC|
|Deposited On:||12 Dec 2013 02:09|
|Last Modified:||17 Mar 2014 03:54|
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